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The understanding of the magnetisation evolution upon femtosecond optical pumping remains elusive. The authors perform resonant X-ray magnetic scattering measurements and multiscale simulations that reveal rapid magnetic order recovery in ferrimagnets via nonlinear magnon processes.

Although magnetostriction is universal in magnetic materials, understanding its microscopic origin remains challenging. Here the authors use X-ray and ultrafast electron diffraction to separate the material’s sub-picosecond spin and lattice responses and reveal the magnetoelastic stress generated by demagnetization.

“The technical support from SLAC Accelerator Directorate, Technology Innovation Directorate, LCLS laser division and Test Facility Division is gratefully acknowledged. We thank S.P. Weathersby, R.K. Jobe, D. McCormick, A. Mitra, S. Carron and J. Corbett for their invaluable help and technical assistance. Research at SLAC was supported through the SIMES Institute which like the LCLS and SSRL user facilities is funded by the Office of Basic Energy Sciences of the U.S. Department of Energy under Contract No. DE-AC02-76SF00515. The UED work was performed at SLAC MeV-UED, which is supported in part by the DOE BES SUF Division Accelerator & Detector R&D program, the LCLS Facility, and SLAC under contract Nos. DE-AC02-05-CH11231 and DE-AC02-76SF00515. Use of the Linac Coherent Light Source (LCLS), SLAC National Accelerator Laboratory, is supported by the U.S. Department of Energy, Office of Science, Office of Basic Energy Sciences under Contract No. DE-AC02-76SF00515.” and “Work at BNL was supported by DOE BES Materials Science and Engineering Division under Contract No: DE-AC02-98CH10886. J.C. would like to acknowledge the support from National Science Foundation Grant No. 1207252. E.E.F. would like to acknowledge support from the U.S. Department of Energy (DOE), Office of Basic Energy Sciences (BES) under Award No. DE-SC0003678.” This has been corrected in both the PDF and HTML versions of the Article.

ObjectivesRight ventricular (RV) failure remains a major concern in heart failure (HF) patients undergoing left ventricular assist device (LVAD) implantation. We aimed to measure the kinetic energy of blood in the RV outflow tract (KE-RVOT) – a new marker of RV global systolic function. We also aimed to assess the relationship of KE-RVOT to other echocardiographic parameters in all subjects and assess the relationship of KE-RVOT to hemodynamic parameters of RV performance in HF patients.MethodsFifty-one subjects were prospectively enrolled into 4 groups (healthy controls, NYHA Class II, NYHA Class IV, LVAD patients) as follows: 11 healthy controls, 32 HF patients (8 NYHA Class II and 24 Class IV), and 8 patients with preexisting LVADs. The 24 Class IV HF patients included 21 pre-LVAD and 3 pre-transplant patients. Echocardiographic parameters of RV function (TAPSE, St', Et', IVA, MPI) and RV outflow color-Doppler images were recorded in all patients. Invasive hemodynamic parameters of RV function were collected in all Class IV HF patients. KE-RVOT was derived from color-Doppler imaging using a vector flow mapping proprietary software. Kruskal-Wallis test was performed for comparison of KE-RVOT in each group. Correlation between KE-RVOT and echocardiographic/hemodynamic parameters was assessed by linear regression analysis. Receiver operating characteristic curves for the ability of KE-RVOT to predict early phase RV failure were generated.ResultsKE-RVOT (median ± IQR) was higher in healthy controls (55.10 [39.70 to 76.43] mW/m) than in the Class II HF group (22.23 [15.41 to 35.58] mW/m, p

Abstract Dehydration accrued during intense prolonged whole‐body exercise in the heat compromises peripheral blood flow and cardiac output (Q˙). A markedly reduced stroke volume (SV) is a key feature of the dehydration‐induced cardiovascular strain, but whether the lower output of the heart is mediated by peripheral or cardiac factors remains unknown. Therefore, we repeatedly quantified left ventricular (LV) volumes, LV mechanics (LV twist, a marker of systolic muscle function, and LV untwisting rate, an independent marker of LV muscle relaxation), left intra‐ventricular pressure gradients, blood volume and peripheral blood flow during 2 hr of cycling in the heat with and without dehydration (DEH: 4.0 ± 0.2% body mass loss and EUH: euhydration control, respectively) in eight participants (three females and five males). While brachial and carotid blood flow, blood volume, SV, LV end‐diastolic volume (LVEDV), cardiac filling time, systemic vascular conductance and Q˙ were reduced in DEH compared to EUH after 2 hr, LV twist and untwisting rate tended to be higher (p = .09 and .06, respectively) and intra‐ventricular pressure gradients were not different between the two conditions (p = .22). Furthermore, LVEDV in DEH correlated strongly with blood volume (r = .995, p

Abstract Background The MOMENTUM3 trial1 has revealed superiority of the novel HeartMate3 (HM3) left ventricular assist device (LVAD) compared with the HM2, with a significantly reduced occurrence of cerebrovascular accidents. Thus, cerebral autoregulation may be improved in HM3 compared with HM II patients, possibly because of altered microcirculatory haemodynamics associated with the in-built speed modulation (‘pulsatility’) of the HM3 device. Methods Angle-corrected Doppler ultrasound images of the middle cerebral artery (MCA) were recorded before and at the end of a 30s breathhold test in healthy controls (n = 17), heart failure (HF n = 18), HM2 (n = 10) and HM3 (n = 17) patients. Microcirculatory haemodynamics as represented by the central retinal artery (CRA) were also quantified (Controls = 33, HF = 27, HM2 = 23, HM3 = 31). Data were analysed for Time-Averaged Maximum flow velocity (TAMAX), peak flow velocity (Vmax), minimum flow velocity (Vmin), Pulsatility Index (PI) and Resistance Index (RI, Table 1). Results Breathhold significantly increased TAMAX, Vmax and Vmin in all groups except HM II patients (Figure 1A). Conversely, PI decreased slightly in all groups while RI was maintained. The greater breathhold response in HM3 compared with HM2 patients was not attributable to the in-built pump-speed modulation (Figure 1B), however, HM3 had a consistently lower RI in the MCA and CRA. Conclusion Although reduced compared with healthy controls, HF and HM3 patients have a significantly greater metabolic cerebral vasoreactivity compared with HM2 patients. The 60% greater diastolic flow velocity in the microcirculation of both LVAD groups compared to healthy controls may alter gas exchange in the microcirculation. Future studies should examine the role of altered RI in HM3 patients. Table 1 Haemodynamics in the middle cererbral artery (MCA) and the central retinal artery (CRA) between HeartMate2 and HeartMate3 patients Healthy controls (n = 33) Heart failure (n = 27) HeartMate II (n = 23) HeartMate3 (average) (n = 31) HeartMate3 (no speed modulation) (n = 31) HeartMate3 (with speed modulation) (n = 31) Middle cerebral artery TAMAX (cm/s) 58 ± 15 48 ± 13 45 ± 15 48 ± 19 48 ± 19 46 ± 18 Vmax (cm/s) 92 ± 22 78 ± 20 55 ± 19*# 55 ± 21*# 54 ± 21*# 55 ± 22*# Vmin (cm/s) 39 ± 12 29 ± 11 37 ± 16 39 ± 14 44 ± 16# 32 ± 13 Pulsatility index 0.88 ± 0.18 1.05 ± 0.31* 0.40 ± 0.24*# 0.34 ± 0.14*# 0.21 ± 0.12*#$ 0.56 ± 0.24*# Resistance index 0.57 ± 0.07 0.60 ± 0.11 0.29 ± 0.14*# 0.16 ± 0.09*#$ 0.17 ± 0.10*#$ 0.14 ± 0.09*#$ Central retinal artery TAMAX (cm/s) 6 ± 1 5 ± 2 6 ± 3 7 ± 3 7 ± 4 6 ± 4 Vmax (cm/s) 12 ± 3 11 ± 6 8 ± 4* 8 ± 4* 8 ± 4* 8 ± 4* Vmin (cm/s) 3 ± 1 3 ± 1 5 ± 2 5 ± 3 6 ± 3*# 4 ± 4 Pulsatility index 1.60 ± 0.45 1.42 ± 0.40 0.58 ± 0.26*# 0.49 ± 0.21*# 0.32 ± 0.17*# 0.79 ± 0.35*# Resistance index 0.75 ± 0.09 0.70 ± 0.11 0.38 ± 0.15*# 0.22 ± 0.11*#$ 0.24 ± 0.12*#$ 0.20 ± 0.13*#$ *p < 0.05 compared with healthy controls; #p < 0.05 compared with Heart Failure; $p < 0.05 compared with HeartMate II. Figure 1 (A) Time-averaged maximum flow velocity in the middle cerebral artery of healthy controls and patient groups in response to a 30-s breathhold test. (B) Breakdown of the responses in HM3 patients, comparing beats with and without added pulsatility.

New Findings What is the central question of this study? What is the role of heart muscle function in the increased output of remodelled, larger hearts? What is the main finding and its importance? The greater stroke volume of endurance athletes is not associated with enhanced function of the heart muscle (i.e. left ventricular twist, torsion and twist‐to‐shortening) in normal and low‐oxygen environments. These data indicate that, in the process of cardiac adaptation, left ventricular twist may play an important role that is not related to generating a larger output. Since enlarged hearts with low output can develop in disease, the present findings may influence the future interpretation of heart muscle function in patients. Abstract Despite increased stroke volume (SV), ‘athlete's heart’ has been proposed to have a similar left ventricular (LV) muscle function – as represented by LV twist – compared with the untrained state. However, the underpinning mechanisms and the associations between SV/cardiac output and LV twist during exercise are unknown. We hypothesised that endurance athletes would have a significantly lower twist‐to‐shortening ratio (TwSR, a parameter that relates twist to the shortening of heart muscle layers) at rest, but significantly greater LV muscle function during exercise. Eleven endurance trained male runners and 13 untrained males were tested at rest and during supine cycling exercise in normoxia and hypoxia (increased cardiac output but unaltered SV). Despite the expected cardiac remodelling in endurance athletes, LV twist, torsion, TwSR, strain and strain rate (‘LV systolic mechanics’) did not differ significantly between groups (P > 0.05). Structural remodelling, as per relative wall thickness, and LV twist did not correlate (r2 = 0.04, P = 0.33). In normoxia and hypoxia, exercise increased LV systolic mechanics in both groups (P

Increased left ventricular (LV) twist and untwisting rate (LV twist mechanics) are essential responses of the heart to exercise. However, previously a large variability in LV twist mechanics during exercise has been observed, which complicates the interpretation of results. This study aimed to determine some of the physiological sources of variability in LV twist mechanics during exercise. Sixteen healthy males (age: 22 ± 4 years, [Formula: see text]O2peak: 45.5 ± 6.9 ml∙kg-1∙min-1, range of individual anaerobic threshold (IAT): 32-69% of [Formula: see text]O2peak) were assessed at rest and during exercise at: i) the same relative exercise intensity, 40%peak, ii) at 2% above IAT, and, iii) at 40%peak with hypoxia (40%peak+HYP). LV volumes were not significantly different between exercise conditions (P > 0.05). However, the mean margin of error of LV twist was significantly lower (F2,47 = 2.08, P < 0.05) during 40%peak compared with IAT (3.0 vs. 4.1 degrees). Despite the same workload and similar LV volumes, hypoxia increased LV twist and untwisting rate (P < 0.05), but the mean margin of error remained similar to that during 40%peak (3.2 degrees, P > 0.05). Overall, LV twist mechanics were linearly related to rate pressure product. During exercise, the intra-individual variability of LV twist mechanics is smaller at the same relative exercise intensity compared with IAT. However, the absolute magnitude (degrees) of LV twist mechanics appears to be associated with the prevailing rate pressure product. Exercise tests that evaluate LV twist mechanics should be standardised by relative exercise intensity and rate pressure product be taken into account when interpreting results.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. The ‘amyloid cascade hypothesis’ assigns the amyloid-beta-peptide (Aβ) a central role in the pathogenesis of AD. Although it is not yet established, whether the resulting Aβ aggregates are the causative agent or just a result of the disease progression, polymerization of Aβ has been identified as a major feature during AD pathogenesis. Inhibition of the Aβ polymer formation, thus, has emerged as a potential therapeutic approach. In this context, we identified peptides consisting of d-enantiomeric amino acid peptides (d-peptides) that bind to Aβ. d-peptides are known to be more protease resistant and less immunogenic than the respective l-enantiomers. Previously, we have shown that a 12mer d-peptide specifically binds to Aβ amyloid plaques in brain tissue sections from former AD patients. In vitro obtained binding affinities to synthetic Aβ revealed a Kd value in the submicromolar range. The aim of the present study was to investigate the influence of this d-peptide to Aβ polymerization and toxicity. Using cell toxicity assays, thioflavin fluorescence, fluorescence correlation spectroscopy and electron microscopy, we found a significant effect of the d-peptide on both. Presence of d-peptides (dpep) reduces the average size of Aβ aggregates, but increases their number. In addition, Aβ cytotoxicity on PC12 cells is reduced in the presence of dpep. [ABSTRACT FROM AUTHOR]